We have demonstrated that desialidated rabbit platelets (which have a short platelet survival) stimulate thrombopoiesis when injected into normal recipients. We plan to study the mechanism of this reaction. Platelets from patients with autoimmune thrombocytopenic purpura (ATP) would be further studied with a radioimmunoassay capable of detecting at the picogram level, surface bound: IgG subclasses, non-IgG antibodies and complement. Platelet membranes would be examined for autoantigens. Lymphocytes from patients with ATP would be studied for their role in the regulation of antibody production and platelet destruction: possible presence of killer cells; possible absence of suppressor cells; interaction of B cells with T cells; and possible lymphocyte dysfunction induced by bound immunoglobulin. We have developed a sensitive quantitative technique, CIE, for the detection of 20 different platelet membrane antigens. We would identify these antigens and employ affinity labeling techniques and CIE for the detection of membrane receptors. Attempts would be made to raise 100% specific, high titer, hybridoma antibodies against specific platelet membrane components. This would facilitate the study of specific membrane components, and contribute to their isolation, characterization, and possible purification. We would also study patients with hereditary and acquired platelet disorders. These studies should provide information on the first stage of platelet function, membrane perturbation.